bat crap crazy

I have posted often about the false claims of scientific reliability and experimental rigor on the part of the Big Pharma and it’s co-conspirators, the Psychology and Psychiatry Industries. I’m not alone.

Right: The primary textbook for brain scan tech and interpretation.

“The low statistical power and the imperative to publish, incentivizes researchers to mine their data to try to find something meaningful,” says Chris Chambers, a professor of cognitive neuroscience at the University of Cardiff. “That’s a huge problem for the credibility and integrity of the field.”

What credibility?

BOLD Assumptions: Why Brain Scans Are Not Always What They Seem

In 2009, researchers at the University of California, Santa Barbara performed a curious experiment. In many ways, it was routine — they placed a subject in the brain scanner, displayed some images, and monitored how the subject’s brain responded. The measured brain activity showed up on the scans as red hot spots, like many other neuroimaging studies.

Except that this time, the subject was an Atlantic salmon, and it was dead.

Dead fish do not normally exhibit any kind of brain activity, of course. The study was a tongue-in-cheek reminder of the problems with brain scanning studies. Those colorful images of the human brain found in virtually all news media may have captivated the imagination of the public, but they have also been subject of controversy among scientists over the past decade or so. In fact, neuro-imagers are now debating how reliable brain scanning studies actually are, and are still mostly in the dark about exactly what it means when they see some part of the brain “light up.”

Glitches in reasoning

Functional magnetic resonance imaging (fMRI) measures brain activity indirectly by detecting changes in the flow of oxygen-rich blood, or the blood oxygen-level dependent (BOLD) signal, with its powerful magnets. The assumption is that areas receiving an extra supply of blood during a task have become more active. Typically, researchers would home in on one or a few “regions of interest,” using ‘voxels,’ tiny cube-shaped chunks of brain tissue containing several million neurons, as their units of measurement.

Early fMRI studies involved scanning participants’ brains while they performed some mental task, in order to identify the brain regions activated during the task. Hundreds of such studies were published in the first half of the last decade, many of them garnering attention from the mass media.

Eventually, critics pointed out a logical fallacy in how some of these studies were interpreted. For example, researchers may find that an area of the brain is activated when people perform a certain task. To explain this, they may look up previous studies on that brain area, and conclude that whatever function it is reported to have also underlies the current task.

Among many examples of such studies were those that concluded people get satisfaction from punishing rule-breaking individuals, and that for mice, pup suckling is more rewarding than cocaine. In perhaps one of the most famous examples, a researcher diagnosed himself as a psychopath by looking at his own brain scan.

These conclusions could well be true, but they could also be completely wrong, because the area observed to be active most likely has other functions, and could serve a different role than that observed in previous studies.

The brain is not composed of discrete specialized regions. Rather, it’s a complex network of interconnected nodes, which cooperate to generate behavior. Thus, critics dismissed fMRI as “neo-phrenology” – after the discredited nineteenth century pseudoscience that purported to determine a person’s character and mental abilities from the shape of their skull – and disparagingly referred to it as ‘blobology.’

When results magically appear out of thin air

In 2009, a damning critique of fMRI appeared in the journal Perspectives on Psychological Science. Initially titled “Voodoo Correlations in Social Neuroscience” and later retitled to “Puzzlingly high correlations in fMRI studies of emotion, personality, and social cognition,” the article questioned the statistical methods used by neuro-imagers. The authors, Ed Vul of University of California in San Diego and his colleagues, examined a handful of social cognitive neuroscience studies, and pointed out that their statistical analyses gave impossibly high correlations between brain activity and behavior.

“It certainly created controversy,” says Tal Yarkoni, an assistant professor in the Department of Psychology at the University of Texas, Austin. “The people who felt themselves to be the target ignored the criticism and focused on the tone, but I think a large subset of the neuroimaging community paid it some lip service.”

Russ Poldrack of the Department of Psychology at Stanford University says that although the problem was more widespread than the paper suggested, many neuro-imagers were already aware of it. “They happened to pick on one part of the literature, but almost everybody was doing it,” he says.

The problem arises from the “circular” nature of the data analysis, Poldrack says. “We usually analyze a couple of hundred thousand voxels in a study,” he says. “When you do that many statistical tests, you look for the ones that are significant, and then choose those to analyze further, but

they’ll have high correlations by virtue of the fact that you selected them in the first place.” We see this again and again in crappy psych “research”

Not long after Vul’s paper was published, Craig Bennett and his colleagues published their dead salmon study to demonstrate how robust statistical analyses are key to interpreting fMRI data. When stats are not done well enough, researchers can easily get false positive results – or see an effect that isn’t actually there, such as activity in the brain of a dead fish.

The rise of virtual superlabs

The criticisms drove researchers to do better work— to think more deeply about their data, avoid logical fallacies in interpreting their results, and develop new analytical methods.

At the heart of the matter is the concept of statistical power, which reflects how likely the results are to be meaningful instead of being obtained by pure chance. Smaller studies typically have lower power. An analysis published in 2013 showed that underpowered studies are common in almost every area of brain research. This is specially the case in neuroimaging studies, because most of them involve small numbers of participants.

“Ten years ago I was willing to publish papers showing correlations between brain activity and behavior in just 20 people,” says Poldrack. “Now I wouldn’t publish a study that doesn’t involve at least 50 subjects, or maybe 100, depending on the effect. A lot of other labs have come around to this idea.”

Cost is one of the big barriers preventing researchers from increasing the size of their studies. “Neuroimaging is very expensive. Every lab has a budget and a researcher isn’t going to throw away his entire year’s budget on a single study. Most of the time, there’s no real incentive to do the right thing,” Yarkoni says.

Replication – or repeating experiments to see if the same results are obtained – also gives researchers more confidence in their results. But most journals are unwilling to publish replication experiments, preferring novel findings instead, and the act of repeating someone else’s experiments is seen as aggressive, as if implying they were not done properly in the first place. Confirmation by repeat experiments is vital to the scientific method!

This “unwillingness” is a SOCIAL IMPOSITION on the validity of scientific inquiry. We wouldn’t want to hurt the feelings of the researchers, would we? But no one cares about the consequences to the public!

One way around these problems is for research teams to collaborate with each other and pool their results to create larger data sets. One such initiative is the IMAGEN Consortium, which brings together neuro-imaging experts from 18 European research centers, to share their results, integrate them with genetic and behavioral data, and create a publicly available database. (Assuming all this “data” is not junk data…)

Five years ago, Poldrack started the OpenfMRI project, which has similar aims. “The goal was to bring together data to answer questions that couldn’t be answered with individual data sets,” he says. “We’re interested in studying the psychological functions underlying multiple cognitive tasks, and the only way of doing that is to amass lots of data from lots of different tasks. It’s way too much for just one lab.”

An innovative way of publishing scientific studies, called pre-registration, could also increase the statistical power of fMRI studies. Traditionally, studies are published in scientific journals after they have been completed and peer-reviewed. Pre-registration requires that researchers submit their proposed experimental methods and analyses early on. If these meet the reviewers’ satisfaction, they are published; the researchers can then conduct the experiment and submit the results, which are eventually published alongside the methods.

“The low statistical power and the imperative to publish incentivizes researchers to mine their data to try to find something meaningful,” says Chris Chambers, a professor of cognitive neuroscience at the University of Cardiff. “That’s a huge problem for the credibility and integrity of the field.”

Chambers is an associate editor at Cortex, one of the first scientific journals to offer pre-registration. As well as demanding larger sample sizes, the format also encourages researchers to be more transparent about their methods.

Many fMRI studies would, however, not be accepted for pre-registration – their design would not stand up to the scrutiny of the first-stage reviewers.

“Neuro-imagers say pre-registration consigns their field to a ghetto,” says Chambers. “I tell them they can collaborate with others to share data and get bigger samples.”

Pushing the field forward

Even robust and apparently straight-forward fMRI findings can still be difficult to interpret, because there are still unanswered questions about the nature of the BOLD signal. How exactly does the blood rush to a brain region? What factors affect it? What if greater activation in a brain area actually means the region is working less efficiently?

“What does it mean to say neurons are firing more in one condition than in another? We don’t really have a good handle on what to make of that,” says Yarkoni.

“You end up in this uncomfortable situation where you can tell a plausible story no matter what you see.”

To some extent, the problems neuro-imagers face are part of the scientific process, which involves continuously improving one’s methods and refining ideas in light of new evidence.(Unless you block the possibility of there being any new evidence.)When done properly, the method can be extremely powerful, as the ever-growing number of so-called “mind-reading” and “decoding” studies clearly show. (Obligatory last sentence contradiction to the theme of the article. Can’t hurt the feelings of the incompetent researchers!)

_____________________________my comment:

That’s just great! In the meantime, hundreds of thousands of children and adults have been “diagnosed” as having abnormal brains and developmental disorders, as well as numerous “mental illnesses” by charlatans, in the “caring, helping, fixing” industry – people who continue to acquire obscene profits at the expense of parents and children who are the targets of borderline “eugenic” activity.

It’s likely that with incremental improvements in the technology, fMRI results will become more accurate and reliable. In addition, there are a number of newer projects that aim to find other ways to capture brain activity. For example, one group at Massachusetts General Hospital is working on using paramagnetic nanoparticles to detect changes in blood volume in the brain’s capillaries.

Such a method would radically enhance the quality of signals and make it possible to detect brain activity in one individual, as opposed to fMRI that requires pooling data from a number of people, according to the researchers.

Other scientists are diving even deeper, using paramagnetic chemicals to reveal brain activity at the cell level. If such methods come to fruition, we could find the subtlest activities in the brain, maybe just not in a dead fish.

Background: DSM-5 sees the introduction of Social (Pragmatic) Communication Disorder (SPCD), characterized by persistent difficulties using verbal and nonverbal communication for social purposes, in the absence of restricted and repetitive interests and behaviours. There is currently much confusion about the precise diagnostic criteria for SPCD and how this disorder relates to autism spectrum disorders (ASD), previous descriptions of pragmatic language impairment (PLI) and more specific language disorders (LD).xMethod: Proposed criteria for SPCD are outlined. A selective review of the evidence considers whether these criteria form a cohesive and distinct diagnostic entity. Approaches to assessment and intervention are discussed. (No one knows if this is a legitimate disorder, but it’s already in the DSM-5 ?)xResults: Implementing the new diagnosis is currently challenged by a lack of well-validated and reliable assessment measures, and observed continuities between SPCD and other neurodevelopmental disorders. High rates of comorbidity between SPCD and other seemingly disparate disorders (including conduct disorder, ADHD and disorders of known genetic origin) raise questions about the utility of this diagnostic category.xConclusions: SPCD is probably best conceptualized as a dimensional symptom profile that may be present across a range of neurodevelopmental disorders, although there is an urgent need to investigate the latent structure of SPCD using consistent diagnostic criteria. In addition, social communication and aspects of pragmatic language may be dissociated, with the latter heavily influenced by structural language attainments. Finally, there is a dearth of reliable and culturally valid assessment measures with which to make a differential diagnosis, and few rigorously tested intervention programmes. The implications for research and clinical practice are outlined.

Enhanced PDF; Standard PDF (139.3 KB) Introduction / Successful communication requires us to go beyond the literal words uttered and draw on our knowledge and experiences to construct meaning. Sometimes this requires the use of linguistic context (pragmatics), in which children are expected to infer meaning or resolve ambiguities by integrating the surrounding language with their prior knowledge and experience. At other times, successful communication requires the use of language in social contexts (social communication). Here, a broad definition would include a child’s understanding of speaker intentions and the verbal and nonverbal cues that signal those intentions, as well as the child’s interpretation of the environmental context, societal norms and expectations and how these coalesce with structural aspects of language (e.g., vocabulary, syntax and phonology) to achieve successful communication. That some children experience difficulties with social communication, or that pragmatic language development can follow a qualitatively atypical course, is incontrovertible. However, the diagnostic status of children with atypical pragmatic and social communication development has long been debated (cf. Brooks & Bowler, 1992), fuelled most recently by the introduction of a new disorder, Social (Pragmatic) Communication Disorder, to the DSM-5 (http://www.psychiatry.org/practice/dsm/dsm5; American Psychiatric Association, 2013a) and proposals for Pragmatic Language Impairment (PLI) to ICD-11 (World Health Organisation, 2013). A resolution of the debate is hampered by inconsistencies in terminology and diagnostic criteria, a paucity of reliable, culturally valid assessment tools supported by adequate normative data, and limited comparison of social communication profiles across different neurodevelopmental disorders.

But that’s never stopped us before, so let’s jump right into a new “fiasco”

The idea that some children may have significant social communication and/or pragmatic language impairments without meeting diagnostic criteria for autism is certainly not new (Bishop & Norbury, 2002); nosologies of developmental disorders have included children with atypical social pragmatic development for more than 30 years. For the most part, investigators have used the terms interchangeably, such that social communication and pragmatic language skills encompass the same behaviours. For instance, Rapin and Allen (1983) first described ‘semantic-pragmaticdeficit syndrome’ as a constellation of symptoms including verbosity, comprehension deficits for connected speech, word finding deficits, atypical word choices, unimpaired phonology and syntax, inadequate conversation skills, speaking aloud to no one in particular, poor topic maintenance and answering beside the point of a question (Rapin, 1996).Wow! is this control-freak creepy or what? Just about any child will display some of these “pathological” speaking habits! Most adults also! xRapin and Allen used this as a descriptive term that was most commonly applied to the communication profiles of children with autism spectrum disorder (ASD), but they acknowledged that social communication and pragmatic language impairments were also seen in many other developmental disorders. Bishop and Rosenbloom (1987) considered ‘semantic-pragmatic disorder’ to represent a distinct subgroup of children who occupied a diagnostic space between ASD and specific language impairment (SLI). Both systems emphasized a deficit in social communication and/or pragmatic language abilities in the context of relatively age-appropriate phonology and grammar. In an effort to improve diagnostic accuracy and interrater reliability, Bishop (1998) created the Children’s Communication Checklist, which has rapidly become the most widely used, standardized measure of pragmatic ability in research and clinical contexts. However, Bishop (1998) reported that semantic items did not reliably distinguish children with suspected social pragmatic deficits from typically developing children or peers with SLI. As a result, the term ‘PLI’ became the generally accepted term for children with primary difficulties in the use of language in context (social or linguistic) who did not meet standard diagnostic criteria for pervasive developmental disorder. However, subsequent research made clear that many children identified with pragmatic deficits using the CCC had structural language impairments (Norbury, Nash, Baird, & Bishop, 2004) and that pragmatic deficits were manifest across a range of neurodevelopmental conditions, some of which involve impairments in general cognitive functioning (cf. Laws & Bishop, 2004). In ASD, deficits in pragmatic aspects of language are a recognized hallmark of the disorder (Tager-Flusberg, Paul, & Lord, 2005). However, children with ASD are commonly identified as having social communication disorders, rather than PLI, perhaps in an effort to emphasize the pronounced difficulties with face-to-face communication individuals with ASD may experience. (Got all that? Make sense? Yikes!)

Why does this debate matter?

The emphasis on identifying and delineating pragmatic and social communication deficits is surely welcome, so could there be any reason to object to the creation of a diagnostic category designed primarily to identify children who might otherwise slip through the net? A revealing use of words – society wouldn’t want a bunch of “communication renegades” running loose! I would argue that there are reasons to be concerned with the diagnosis in its current form, particularly as diagnosis typically carries with it a promise of tailored intervention and educational support. As differences in terminology highlight, there is considerable confusion surrounding the new diagnosis, and the different perspectives of the clinical practitioners who will be charged with making it. There is particular concern about the inclusion and possible exclusion criteria, which may mean that few individuals actually meet diagnostic criteria. This is complicated by clear overlaps with the diagnostic criteria for language disorder and ASD, making differential diagnosis particularly challenging. There is also legitimate concern that children receiving this diagnosis would not receive the clinical or educational services that they may require. It has been documented that federal funding for research into ASD far outstrips that for language disorder (Bishop,2010) and that children with ASD receive far more intensive and consistent educational support for language than peers with language disorder, even when the latter group have more severe language impairments (Dockrell, Ricketts, Palikara, Charman, & Lindsay, 2012).

In this review, I will outline proposed criteria for SPCD and consider the evidence that SPCD is a valid diagnostic construct. Most of the research I will review previously identified nonautistic children with social communication deficits as having PLI, although children with structural language impairments were not always excluded from these studies. For consistency, I will use the term SPCD to refer to the children included in past studies. However, I will argue that social communication and pragmatic language skills are not necessarily one and the same, with the latter closely associated with structural aspects of language. I will argue that to assess and treat SPCD, it is vital to understand the continuities between SPCD and both ASD and language disorder, as well as consider the high rates of comorbidity between SPCD and other developmental disorders. Finally, I will argue that as with most neurodevelopmental disorders, SPCD is best conceptualized along a set of symptom dimensions, rather than as a discrete categorical entity, although there is an urgent need to empirically establish the symptom profile that is associated with social pragmatic deficits in the absence of autism. ESPECIALLY SINCE IT’S A “DONE DEAL” IN THE DSM-5

DSM-5 criteria for social (pragmatic) communication disorder (SPCD)

One reason for the inclusion of SPCD within DSM-5 and PLI in ICD-11 is the well-publicized changes to criteria for autism and related conditions, and the potential impact of these changes on provision for individuals who no longer meet criteria for ASD (Aha! The real reason for “invention” of this disorder and inclusion in the DSM-5 is political; now we have to put lipstick on this pig.) (Huerta, Bishop, Duncan, Hus, & Lord, 2012; McPartland, Reichow, & Volkmar, 2012). Whereas previous diagnostic frameworks specified a triad of impairments, the new systems will focus on twosymptom dimensions: social communication deficits and restricted and repetitive interests and behaviours(isn’t the latter “repetitive” stuff supposedly a symptom of ASD? (see Lord & Jones, 2012 for discussion). There have been discrepant estimates of how many individuals with existing diagnoses would still warrant a diagnosis of ASD under the new classification. For example, McPartland et al. (2012) reported that only 60.6% of participants with a current diagnosis would meet new criteria for ASD, whereas Huerta et al. (2012) reported that 91% of their sample would retain their current diagnosis (although specificity in this sample was remarkably low at .53).(Holy Crap! Could the DSM be any LESS medically or scientifically legitimate?)

A shameless conspiracy of “symptoms” selected and organized to match invented disorders! It’s as if these “experts” are fighting over the seating chart at a political dinner!

Neither study was able to establish how many individuals would meet criteria for SPCD as the operational criteria for the new disorder are currently rather limited. However, Huerta et al. (2012) reported that only 1.5% of their participant pool met social communication criteria for ASD, but did not meet threshold criteria for RRIBs.

Such studies give rise to the concern that SPCD will be treated as a residual category for ‘not-quite’ ASD, rather like the previous PDD-NOS category (Skuse, 2012). A definition by exclusion could be particularly problematic as SPCD will come under the umbrella of Communication Disorders, a set of disorders that are typically the remit of speech-language pathologists. In this arena (in case you doubt that these are turf wars) restricted and repetitive interests and behaviours are not routinely assessed and definitively ruling out ASD may prove challenging.

Table 1 outlines inclusion criteria for SPCD (American Psychiatric Association, 2013b): Previous draft criteria acknowledged that SPCD could co-occur with disorders other than ASD, such as language disorder or intellectual disorder, but stipulated that social communication deficits could not be explained by deficits in vocabulary, grammar or general cognitive ability. Notably, current draft criteria for PLI in ICD-11 stipulate exclusion of both ASD and receptive/expressive language disorders. (Aye, yai, yai!)

The following text / charts are examples of utterly irrational NEUROTYPICAL NUTTINESS: The “magic word” illusion that plagues NTs detaches their “thinking” from reality.

What do ‘diagnostic’ WARS have to do with real specific children? NOTHING. We’re talking about trivial social interactions (Have a Nice Day!) that are cultural defined and pertain to shallow repetitive NONCOMMUNICATION.

Skuse (2012) raised a number of pertinent concerns about the SPCD diagnosis. First and foremost is how these diagnostic criteria will be operationalized and defined in such a way that they do not amount to ASD equivalent social and pragmatic deficits in the absence of restricted and repetitive interests and behaviours (RRIBs). Here, it may be helpful to consider whether SPCD is underpinned by the same cognitive constraints in different diagnostic groups. In ASD, there is an overriding assumption that SPCD is a consequence of core deficits in social cognitive processes such as theory of mind, while in other developmental populations, SPCD may occur in the absence of social cognitive deficit. Whether differences in the cognitive origins of SPCD yield qualitatively different communication profiles is an open question. A second concern is whether there is any evidence that children with SPCD form a coherent and etiologically distinct group, requiring a different course of intervention or educational support. A related issue is the developmental course and diagnostic stability of SPCD; at what point can a diagnosis be made reliably and how does the phenotype change over time? Finally, Skuse (2012) queries whether the presence of RRIBs yields a qualitatively distinct social communication profile, or confers more functional impairment relative to SPCD in isolation. In a similar vein, I suggest that it would be unwise to assume that co-occurring language and intellectual impairments necessarily cause SPCD, given the intimate developmental relationships that exist between social, linguistic and cognitive achievements (Chiat & Roy, 2008). We need to know much more about how individual differences in each of these developmental pathways influence social communication development and disorder.

To begin to answer these questions, however, we need to identify the relevant children. Below, I outline best practices for assessment of social communication and pragmatic language abilities and highlight some of the difficulties in measuring these skills. I will then consider differential diagnosis of SPCD from ASD and Language Disorder, as well as the presence of SPCD in other neurodevelopmental disorders.

Assessment and diagnosis of social communication and pragmatic language skills

Social communication and pragmatic language abilities are notoriously difficult to measure in standardized ways because they are a set of contextually dependent human behaviours that occur in dyadic exchanges; the structure provided by a standardized testing situation makes it difficult to capture social communication problems that may arise in everyday situations where the rules of engagement are less explicit and highly dynamic (Adams, 2002; Volden, Coolican, Garon, White, & Bryson, 2009). Social communication skills are also highly susceptible to cultural variation: discourse rules such as turn taking, interrupting, appropriate topic choices, use of eye contact and other nonverbal strategies for maintaining interaction, use of humour, and the ability to question and challenge communication partners, are largely determined by cultural rules and the child’s relationship with his or her interlocutor (Carter et al., 2005). Unlike structural aspects of language (e.g., vocabulary or grammar), there are also far fewer normative data for such behaviours (Norbury & Sparks, 2013).

Adams (2002) provided a summary of developmental social communication and pragmatic attainments and a detailed examination of popular methods for assessing these skills. A brief overview is provided below and in Table 2, focusing on methods of assessing conversational skill, narrative ability and the understanding/use of ambiguity (i.e. inferencing, multiple meanings and figurative language). Measures are organized according to the method of assessment, including checklist or rating scale, structured observation and formal assessments with pragmatic content.

Unusual in that it does not involve a retelling and so may be more sensitive to social pragmatic deficits

Parent teacher report of children’s communication

Given the inherent difficulties of extrapolating pragmatic performance in clinical settings to everyday communicative competencies (Volden et al., 2009), standardized checklists of pragmatic and social communication behaviours have become a popular method of assessment. The Children’s Communication Checklist (CCC, Bishop, 1998; CCC-2, Bishop, 2003a, 2003b) is perhaps the most widely used checklist in clinical practice and research. The CCC-2 is a 70-item checklist comprised of 10 scales; eight scales tap structural and pragmatic language and two scales measure the social impairments and restricted interests more typical of ASD. Normative data are available on over 500 UK children and over 900 US children aged 4 to 17 years and it has been translated into more than 30 different languages. Respondents are asked to rate the frequency of communication behaviours on a four-point scale. In the original CCC, a pragmatic composite was derived by summing the scores of scales that tapped pragmatic language competence. These included inappropriate initiation, coherence, stereotyped language, use of context and conversational rapport. However, in the validation sample, this composite score had poor levels of interrater reliability and was not successful at discriminating children identified as having PLI from children with diagnoses of more specific language impairment (Norbury et al., 2004). One reason is that children with SLI obtained low scores on the pragmatic composite, highlighting an association between structural language and pragmatic language skill that has been consistently replicated (cf. Ketelaars, Cuperus, van Daal, Jansonius, & Verhoeven, 2009; Volden et al., 2009).

To address this issue, Bishop (2003a, 2003b) devised the Social Interaction Deviance Composite (SIDC), which identifies pragmatic abilities that are disproportionately impaired relative to structural language competencies. Thus, a positive score indicates relatively mild pragmatic difficulties in conjunction with more severe deficits in structural language. Scores around zero are indicative of a child with equally severe pragmatic and structural language deficits (i.e., a significant proportion of children with ASD) and negative scores would be more consistent with a profile in which scores on structural language tests were within normal limits, but the child experienced pronounced social communication deficits. An important caveat is that amongst a large cohort of children with communication disorders, scores on the SIDC were continuously distributed, with no clear categorical boundaries between specific language impairment, SPCD or ASD (Norbury et al., 2004). Therefore, the CCC-2 should be used to signpost aspects of communication for further assessment, rather than providing a clear diagnosis itself.

In addition to parent or teacher report measures, clinicians may wish to rate aspects of a child’s communicative behaviour more directly. Three main criteria for SPCD centre on the individual’s conversational skills, specifically initiation and response to conversational bids, adapting conversation to listener needs and environmental expectations and following conversational rules, such as turn taking. Quantitative approaches to analysing conversation in detail have been developed with acceptable levels of interrater reliability (Bishop & Adams, 1989). Conversational analysis may also provide an ecologically valid tool with which to demonstrate improvements in pragmatic and social communication competence following intervention (Adams, Lloyd, Aldred, & Baxendale, 2006). Despite these advantages, it remains a time-consuming assessment method, which may limit its clinical and research utility. Measures such as the Targeted Observation of Pragmatics in Children’s Conversation observation scale (Adams, Gaile, Freed, & Lockton, 2010) shows promise as a method of rating the quality of conversational exchanges, and is sensitive to developmental change (Adams et al., 2012). However, there is little research at present regarding its diagnostic sensitivity and specificity.

Structured observation

An advantage of structured observations is that the examiner can create naturalistic contexts specifically designed to elicit social communication behaviours, thus judging whether or not they occur and whether there are qualitative differences in the child’s communicative behaviours. ‘Conversational’ behaviours can also be assessed prior to the advent of spoken language. Three measures, the Early Social Communication Scales (Mundy et al., 2003), the Communication and Symbolic Behavior Scales (Wetherby & Prizant, 1993) and the Autism Diagnostic Observation Schedule (ADOS)-Toddler Module (Luyster et al., 2009) assess how infants and toddlers initiate and respond to interactions with adults. This may include observation of whether the child uses eye gaze, gesture or vocalizations to gain the adult’s attention, direct attention or respond to a direct request. Such measures usually include ‘presses’, which attempt to elicit specific communicative acts. For example, the child might be shown a very tempting wind-up toy. After demonstrating what the toy can do, the examiner will hold back and wait to see whether and how the child obtains help from an adult to make the toy move again. For older children and adolescents, measures such as the ADOS and ADOS-2 (Lord, Rutter, DiLavore, & Risi, 2001) and the Yale in vivo Pragmatics Protocol (Schoen & Paul, 2009) include more sophisticated ‘presses’ including observation of how the child greets an unfamiliar adult, whether the child spontaneously offers information about his/her own experiences and how the child integrates verbal and nonverbal (e.g., eye gaze, gesture) communication behaviours.

A rather blunt measure of conversational skill is also included in the ADOS (Lord et al., 2001). Here, the examiner attempts to engage the individual in a conversational exchange, providing ‘hooks’ to which the child is expected to comment or question the examiner further. The conversation is scored on a 4-point scale, with a score of 3 indicating total absence of conversation, and a score of 0 representing a conversation that has at least four coherent turns (e.g., examiner comments, child questions, examiner responds and child comments). Separate codes tap quality of initiations or response, use of facial expression and gesture, and the integration of verbal and nonverbal information for communicative purposes.

One strength of structured observations such as the ADOS is that they provide a consistent context in which to observe qualitatively different or unusual communication behaviours. A limitation of these assessments is that there are few normative data available on which to make judgements of conversational adequacy. Modules 3 and 4 of the ADOS cover a wide age range from 4 years to adulthood. While typically developing four-year olds are capable of sophisticated conversational exchanges, we might expect qualitative differences between conversational skills of children and adults. In addition, the degree to which children feel able to comment or question unfamiliar adults is culturally dependent (cf. Norbury & Sparks, 2013).

Formal assessments with pragmatic content

Narrative analysis constitutes an important tool for revealing pragmatic deficits, as it taps the integration of linguistic, cognitive and social pragmatic abilities. Narrative measures allow assessment of the child’s ability to convey a coherent sequence of events, provide the right amount of key information to the listener and use cohesive devices consistently. In addition, unusual or bizarre comments thought to be indicative of ASD may be revealed, although interrater reliability of ‘bizarre’ comments can be disappointingly low (Norbury & Bishop, 2003) and are present in only a minority of ASD narratives (Norbury, Gemmell, & Paul, 2013). Several standardized assessments of narrative exist, including the Bus Story (Renfrew, 1995), the Expression, Reception and Recall of Narrative Instrument (Bishop, 2003a,2003b) and the Strong Narrative Assessment Procedure (Strong, 1998). Less formal assessment measures include telling a story from a picture book (Norbury & Bishop, 2003) or generating narrative in response to a story stem (Demir, Levine, & Goldin-Meadow, 2010).

Narrative is an important part of clinical assessment not least because it is a foundational skill for academic achievement (Boudreau, 2008). However, narrative skills are vulnerable across a range of developmental disorders and direct comparisons of different clinical populations have yielded few quantitative or qualitative differences in narrative performance (Norbury & Bishop, 2003; Norbury et al., 2013; Finestack, Palmer, & Abbeduto, 2012). Furthermore, measures of structural language ability are typically the strongest predictors of narrative competence within clinical populations (Kay-Raining Bird, Cleave, White, Pike, & Helmkay, 2008).

More direct assessment of pragmatic language ability may also include measures of inferencing, understanding of humour or figurative expressions such as metaphor, idiom or irony, and referential communication, including the child’s ability to request clarification or identify messages that are ambiguous or underinformative. Standardized measures, such as the Test of Language Competence (Wiig & Secord, 1989) or the Test of Pragmatic Language-2nd Edition (Phelps-Terasaki & Phelps-Gunn, 2007) have distinguished groups of children with known pragmatic deficits from comparison groups (Young, Diehl, Morris, Hyman, & Bennetto, 2005). However, Adams (2002) argues that such formal testing measures are unlikely to reveal an accurate or comprehensive picture of the child’s pragmatic competence in more dynamic, context dependent communicative exchanges.

Social communication and pragmatic language: same or different?

Social (Pragmatic) Communication Disorder criteria stipulate that impairments should be evident in all four of the aspects of communication specified: using communication for social exchange, adapting communication style to the context, following rules of conversation or narrative convention and understanding implicit or ambiguous language. It would appear that this requirement presumes that social communication and pragmatic language skills are manifestations of the same underlying cognitive process(es). Indeed, these skills are closely associated; a recent population study demonstrated that pragmatic language skills were highly predictive of social competence, even after expressive language abilities had been taken into account (Ketelaars, Cuperus, Jansonius, & Verhoeven, 2010). However, there is mounting evidence that even within the autism spectrum, social communication deficits and pragmatic language impairments may be dissociated, and can arise from different underlying constraints.

Traditionally, social pragmatic impairments in ASD have been attributed to the absence or attenuation of the social instinct (Wing, Gould, & Gillberg, 2011) and a fundamental impairment in ‘theory of mind’ (Baron-Cohen, Leslie, & Frith, 1985). A lack of social motivation can readily explain conversational impairments such as a lack of initiation or minimal contingent responses. Reduced experience with social interaction may alter the course of pragmatic development, in that it limits exposure to nonverbal communicative gestures (facial expression, gesture) and the flexible nature of language use. Social cognitive deficits are hypothesized to lead to reduced ability to represent a listener’s state of mind; this could contribute the recognized limitations in providing the appropriate amount of information to minimize ambiguities in conversation (Capps, Kehres, & Sigman, 1998; Tager-Flusberg & Anderson, 1991) or conveying sufficient information of interest to the listener in conversation and narrative tasks (Capps, Losh, & Thurber, 2000). Difficulties understanding speaker intentions have also been attributed to reported deficits in understanding figurative language such as metaphor and irony (Happé, 1993; Martin & McDonald, 2004), and deficits in referential communication (Nadig, Vivanti, & Ozonoff, 2009).

However, it is important to realize that there is usually considerable variation within ASD groups on these tasks and that social communication abilities have been linked not only to mentalizing, but are often associated with structural language abilities (see Gernsbacher & Pripas-Kapit, 2012 for discussion in relation to figurative language). For instance, Norbury (2005) investigated metaphor comprehension in children with ASD and compared those with additional language impairments (ALI) with those who scored within normal limits on assessments of structural language competence (ALN). Notably, these groups did not differ with respect to social communication deficit, as measured by the Social Communication Questionnaire (Rutter, Bailey & Lord, 2003), nor do they typically differ on ADOS or Vineland Adaptive Behavior Scales social indices (cf. Norbury et al., 2009). Children with ALN did not differ from typically developing peers on the metaphor task, whereas those with ALI had significantly lower scores. Moreover, scores on measures of structural language predicted unique variance in metaphor understanding, whereas scores on Theory of Mind tasks did not.

Furthermore, studies employing experimental measures of inferencing ability and ambiguity resolution have found few differences between individuals with ASD and typically developing peers, providing the individuals with ASD had age-appropriate structural language abilities (Brock, Norbury, Einav, & Nation, 2008; Norbury, 2005; Pijnacker, Hagoort, Buitelaar, Teunisse, & Geurts, 2009). Structural language abilities reliably predict performance on these tasks, even within ASD populations (Volden et al., 2009). Thus, it would seem that social communication deficits may be evident in children who are indistinguishable from TD peers on measures of pragmatic language functioning.

Social communication undoubtedly draws on a number of skills, of which social cognition (as measured by theory of mind tasks) is just one. And it is possible that a stronger relationship would be found between social communication and pragmatic language abilities if different tasks were employed to measure pragmatic language skill. Nevertheless, the studies cited above suggest that to require both social and pragmatic deficits to be present may preclude diagnosis in young people with average or above average structural language skills. Conversely, those most likely to demonstrate impairments in both are very likely to have additional impairments in word knowledge and grammar, which may also preclude diagnosis.

Differential diagnosis of SPCD

Is SPCD a milder form of ASD?Crucially, DSM-5 and ICD-11 will require that children with SPCD do not exhibit clinically significant RRIBs. There has been some disagreement in the literature regarding the extent to which children identified as having primary SPCD show evidence of RRIBs. Reisinger, Cornish, and Fombonne (2011) explicitly compared children with ASD and children with SPCD on the ADOS and the SCQ. They found that the groups could be distinguished by the severity of social and communication deficits, but did not differ significantly on measures of RRIB. In contrast, Bishop and Norbury (2002) used similar methods and reported that children with SPCD as a group were less likely to display RRIBs. However, the majority of children with SPCD were rated as having speech abnormalities associated with autism and used stereotyped language. In addition, a significant minority were reported to have unusual sensory interests. Changes to DSM-5 criteria for ASD include the reclassification of stereotyped language as an RRIB, rather than a communication symptom, and include sensory interests. Thus, many of the children studied by Bishop and Norbury (2002) may meet new DSM-5 criteria for ASD.

These studies used the ADOS and the SCQ to quantify RRIB; the reliability of these algorithms is low (Lord et al., 2000) and the scales are perhaps not detailed enough to identify differences between diagnostic groups. A recent study by Gibson, Adams, Lockton, and Green (2013) utilized the Repetitive Behaviour Questionnaire-2 (Leekam et al., 2007) and reported that children with SPCD could be distinguished from peers with ASD on this measure. However, the children included in this study were young, aged between 6 and 11 years. A complication for differential diagnosis is that symptom profiles may change significantly with age (Bishop & Norbury, 2002; Howlin, Mawhood, & Rutter, 2000), with an increase in specialist interests and rigid behaviour becoming more evident over developmental time. Thus, a group difference in the early school years may be less apparent in adolescence. A further complication is that few studies have measured RRIBs in children with SPCD in relation to typically developing peers. It is likely that even if children with SPCD do not exhibit enough RRIBs to meet threshold for ASD, they have elevated levels of RRIB relative to peers. In short, it may not be possible to distinguish ASD and SPCD on the basis of behavioural profiles alone (Reisinger et al., 2011).

Is SPCD a form of Language Disorder?

DSM-5 criteria for Language Disorder stipulate that children will have impairments in any one of three areas: word knowledge, grammar and discourse. Discourse includes narrative and conversational exchange, thus overlapping with SPCD. Children with more ‘specific’ forms of Language Disorder have variable social interaction and social communication difficulties relative to TD peers. These may include difficulties establishing social relationships (Whitehouse, Watt, Line, & Bishop, 2009); poorer quality friendships (Durkin & Conti-Ramsden, 2007); difficulties with peer negotiation and conflict (Brinton, Fujiki, & McKee, 1998; Horowitz, Jansson, Ljungberg, & Hedenbro, 2006) and poorer social cognition (Marton, Abramoff, & Rosenzweig, 2005). In general, it is argued that these social deficits are secondary to the language impairment and strong associations between language test performance and measures of social deficit support this view (Gibson et al., 2013). However, measures do not always correlate, and there is some suggestion that social deficits might be concomitant with language impairment (Marton et al., 2005). It is also typically the case that on measures of social competence, there is a pattern of increasing severity in which children diagnosed with ASD demonstrate the most severe social impairments, children with language disorder the mildest deficits and children with SPCD falling between the two (cf. Gibson et al., 2013). Often performance is continuously distributed with little clear indication of where diagnostic boundaries lie.

Difficulties with pragmatic aspects of language are more consistently vulnerable in children with language disorders. For instance, compared with age-matched peers, children with ‘specific’ language impairment have deficits in narrative (Norbury et al., 2013), inferencing (Katsos, Roqueta, Estevan, & Cummins, 2011), figurative language comprehension (Norbury, 2005) and the use of language context to resolve ambiguities (Brock et al., 2008). Furthermore, distinguishing children with language disorders from those with SPCD on these sorts of pragmatic tasks has met with little success, typically because of the poor performance of children with language impairment. At a group level, differences have been reported in the severity of expressive language disorder (with SPCD experiencing less severe impairments) and in the severity of peer social difficulty (Gibson et al., 2013). However, this is not always the case and the distinction between the two remains one of degree (Norbury et al., 2004).

The clearest evidence for a distinction between language disorder and SPCD comes from detailed analyses of conversational adequacy (Adams & Bishop, 1989; Bishop & Adams, 1989; Bishop, Chan, Adams, Hartley, & Weir, 2000). In these studies, children with SPCD were more likely than language-impaired peers to violate turn-taking expectations, provide no response or pragmatically inappropriate responses to conversational overtures, and made little use of nonverbal communicative devices. Such studies emphasize the importance of measuring social communication in naturalistic conversational exchanges (Adams & Lloyd, 2005). However, the strength of group difference rests with the diagnostic profiles of the children with SPCD. Clearly, DSM-5 criteria were not employed in these studies and it is possible that the more severely impaired children may have met DSM-5 criteria for ASD (Bishop, Whitehouse, Watt, & Line, 2008). Given that the new diagnostic criteria focus so heavily on dyadic conversational exchanges, developing an appropriate analysis measure and honing in on aspects of conversation that yield stable, qualitative differences is an important priority for future research.

There is intense research and clinical interest in using the CCC/CCC-2 to identify qualitatively different social communicative profiles that align with specific clinical diagnoses, with varying success. For example, Bishop and Baird (2001) reported that the CCC identified pragmatic deficits in children with pervasive developmental disorders, primary pragmatic language impairments and children with ADHD, but that there were no significant differences amongst the clinical groups in pragmatic profile. On the other hand, Geurts et al. (2004) reported that children with ADHD had more severe deficits on items tapping initiation relative to peers with ASD, while those with ASD had more impaired scores on scales tapping structural language and RRIB. Philofsky et al. (2007) reported that children with William’s syndrome had significantly better scores on CCC scales tapping coherence, stereotyped language, nonverbal communication and social relations relative to peers with ASD. However, it is important to bear in mind that most of the differences between clinical groups are a matter of degree and are reported at a group level. There remains much work to be carried out on the sensitivity and specificity of particular pragmatic profiles for differential diagnosis. In addition, clinical groups often differ with regard to structural language, social understanding, cognitive ability and the presence of other developmental concerns such as attention deficits, executive dysfunction and behavioural difficulties, all of which are strongly associated with social and pragmatic deficits (Ketelaars et al., 2009; Mackie & Law, 2010). Individual differences in social communication and pragmatic language are therefore likely to reflect a confluence of risk factors in each of these developmental areas. How these factors interact over time to affect social interaction and contextual processing is an empirical question. It is therefore unlikely that there is a syndrome-specific social pragmatic profile. Instead, there will be individual variation associated with the particular constellation of risk factors that the child experiences. One may hypothesize that ASD represents the extreme end of the distribution in which multiple risk factors are present, creating the least favourable conditions for pragmatic language and social communication to develop.

Clinical and educational implications: treatment

One advantage of creating a new diagnostic category is that it should indicate a specific course of treatment or educational support. If we identify SPCD as a clinical disorder, treatment is likely to be aimed at improving social communication outcomes, to foster improvements in social relationships and to prevent negative consequences such as disruptive behaviour and social withdrawal. There is a paucity of good quality intervention research, in part hampered by inconsistencies in diagnostic labels, lack of agreement concerning diagnostic criteria and valid instruments for measuring change (Gerber, Brice, Capone, Fujiki, & Timler, 2012). Adams et al. (2012) reported the first randomized controlled trial of a social communication intervention aimed specifically at children with SPCD. The Social Communication Intervention Project (http://www.psych-sci.manchester.ac.uk/scip/) is an individualized intervention approach that targets development in three areas: social understanding and social interaction; verbal and nonverbal pragmatic skills, including conversation; and language processing, including narrative, inferencing, and developing word knowledge. In the trial, 88 children with SPCD were randomly assigned to the intervention or treatment as usual. After 20 sessions of intensive intervention by a highly specialist speech-language therapist, significant treatment effects were reported for ratings of conversational competence (blind ratings), parent ratings of pragmatic skill and social communication (not blind) and teacher ratings of classroom learning (not blind). No significant treatment effects were seen for the primary outcome measure (the Clinical Evaluation of Language Fundamentals -4UK, Semel, Wiig, & Secord, 2003) or a test of narrative expression.

The study is very promising in demonstrating that observable differences in social communication behaviour can be achieved after a period of intensive intervention. However, there are clearly many challenges to overcome. Study participants were extremely heterogeneous, varying from the 3rd to the 95th percentile on all measures of structural language, nonverbal reasoning, and ASD symptomatology. Such extreme within-group differences make it difficult to discern treatment effects. In addition, the outcome measure bore little relationship with the treatment content or treatment aims. Treatment most commonly aims to optimize language and communicative function rather than ‘cure’ disorder. In that regard, it is unlikely that diagnostic instruments themselves are sensitive enough to show change. However, the need for standardized assessment of social communicative function is great and a top priority for future research. Given the complexities of social communication and pragmatic language, it is also perhaps unrealistic to think that we can expect significant change in a relatively brief period of intervention. It is likely that these children will require on-going support as they get older and the complexity of social communication and language context increases in the expectation for more intimate social relationships, and for using language for learning and employment.

Summary and future directions

At present, there is too little research evidence to fully support a new diagnostic category, or to help identify aspects of social communication that distinguish SPCD from other developmental conditions. Social communication disorders and pragmatic language impairments constitute a broad range of phenomena that are likely to be continuous in nature and influenced by a number of developmental achievements. Social communication and pragmatic language skills are not necessarily one and the same; if pragmatics is taken to be the understanding and use of language in context, many children will succeed at pragmatic language tasks such as inferencing and ambiguity resolution and yet be challenged by the nuances of successful social communication.

To establish the validity of SPCD as a diagnostic entity, clinical research must (1) describe a coherent clinical phenomenon; (2) develop culturally and ecologically valid assessment tools with adequate levels of interrater and test–retest reliability to improve consistency of diagnosis; (3) explicitly compare pragmatic profiles across different neurodevelopmental disorders; (4) chart the developmental trajectories of children with SPCD and monitor the stability of diagnosis over time; and (5) conduct family studies to begin to unravel the aetiology of this disorder and its relation with other neurodevelopmental conditions (cf. Robins & Guze, 1970). In addition, intervention studies are urgently needed as they will offer a means to test theories regarding the putative causes and consequences of social (pragmatic) communication disorders.

Clinical implications

Differential diagnosis of SPCD will be challenging, but the focus on social communication and pragmatic language abilities should be welcomed. Many children presenting for psychological or psychiatric assessment will have some degree of pragmatic language or social communication deficit (Cohen, Farnia, & Im-Bolter, 2013; Cohen et al., 1998) that will require specialist treatment and support. It would therefore seem prudent to obtain parental report of communication skills in everyday contexts, for example using the CCC-2 (Bishop, 2003a, 2003b). Such a measure can inform hypotheses and assessment plans; where there is evidence of a significant social pragmatic deficit, evaluation for ASD will also be essential. On the CCC-2, an index score of zero indicates that both structural and pragmatic language impairments may be evident; thus, an evaluation by a speech-language therapist for language disorder will be necessary. Although standardized measures for exploring pragmatic aspects of language exist, these may not reflect the individual’s ability to apply these skills in less formal settings. Observations of naturalistic interaction, in school or at home, may be most informative. Finally, intervention is likely to be multifaceted, incorporating techniques for improving social understanding and social interaction, structural aspects of language (e.g., vocabulary) and using linguistic context to improve comprehension. Thus, intervention should be centred on the profile of strength and need that emerges from the assessment process, rather than the diagnostic label obtained.

Acknowledgement

The open access fee for this article has been funded by the Economic and Social Research Council (ESRC). This review article was invited by the Editors of JCPP, for which the author has been offered a small honorarium towards personal expenses. The author has declared that she has no competing or potential conflicts of interest.

Below:A standard “analogy” in basic physics courses: Does this really make “electricity-magnetism” accessible to the average student?

The problem is, that even basic physics courses assume that the student has “hung out” at the local water plant or was raised by a plumber. If not, the added water system analogy means that the student now must understand the water system in addition to struggling with the electrical system.

Water wheels, grindstones? A bit archaic, no?

Okay – so the water system analogy isn’t terrible, but here is where the use of analogy drives me bonkers: number, quantity, volume, weight, density, forces …. Comparisons to strange objects are believed to make extremes of number and scale “comprehensible” to the human brain. Again – the assumption is that “equivalents” such as the earth covered in marbles or peas to some “impressive” depth is: 1. meaningful 2. has a possibility of occurring outside of a supernatural “miracle” 3. will ever be observed by one or more human beings. 4. will reduce the problem of incomprehensible quantity, number, etc in comparison to “human” scale.

But, “1/18th of the surface area of the sun” makes “Avogadro’s Number” perfectly clear! What was it we were trying to explain? I’ve forgotten, and I have a headache.

Another terrific assumption is that Olympic swimming pools and football fields are perfectly reasonable examples of “intuitive” volumes and areas because everyone has watched the Olympics on TV or has been to a football game.

And a more problematic question: Why are we presenting students with ridiculous analogies for actual measurable physical phenomenon, when the function of teaching science and technology is to impart awareness and knowledge of “How the universe works” ? What we’re telling them is that physical properties, relationships and behaviors are baffling; that physical reality measurements are fantastical and incomprehensible. And why must we understand measurements in “relatable ways” at all? Isn’t that a function of mathematics – to make the humanly “ungraspable” available and easier to work with?

While science education is making physical reality (that we occupy and depend on) “obscure and incomprehensible” religions and politicians are doing the opposite:

Is it any mystery as to why millions of Americans believe that climate change, global warming and other major systemic problems are “government conspiracies?”

And in case one might imagine that biology and other areas are any less idiotic:

Like this:

One of my enduring “analytical” interests is how language is used to construct social reality.

I have been looking into how “Autism, the Epidemic” is being publically constructed and promoted.

A pattern is obvious: take any human behavior (even if it’s widespread and previously acknowledged as within the normal range for humans – or even essential to human development)and redefine it as a symptom of pathology. Gather together a list of these various symptoms, which are presented as evidence that something is wrong with your child; “symptoms” for which the criteria are vague and mostly subjective and repetitive, but with no factual basis for a coherent connection between them: add these to a few “legitimate” difficulties, such as learning disabilities, motor difficulties, behavior problems, for which the criteria are also vague and mostly subjective and repetitive – perhaps “annoying” is the common denominator – Collect these together and present them as a “newly discovered disorder”. Legitimize it by voting it into the latest version of the DSM. (Who decides what goes into the DSM?)

This act of construction may be all that connects the supposed symptoms; that is, there is no objective basis for the existence of a common or causal link except for the “naming” of a new disorder. The disorder has been “created” by repurposing existing symptoms from other disorders to expand the pool of official pathologies, which creates the illusion of something real and new is going on: The Autism epidemic.

Once the disorder is promoted by “studies” – many of which are nothing more than a favorably reinterpreted review of former studies,selected and manipulated into “proving” a pre-decided outcome. Studies which may have no value; which may be spurious, phony, published with no peer review (as if that may mean anything anymore)and funded by corporate interests and institutions, in order to get the “results” that they have paid for. The result is that Autism is a “collage” of mysterious manifestations; diagnosis are meaningless opinions with no medical basis; a mish-mash controlled by the Autism industry and insurance companies. The rush to diagnosis is driven by media “fads” and advertising. Fear sweeps the public and drives profits.

Typical of this process is the expansion of a behavior or trait from its original narrow and restricted definition(which originated as a medical or descriptive usage)into the realm of psychosocial application; this is often justified by the supposed “consequences” of the condition – depression, anxiety and interference in any and all life activities, including for Autistic disorders, a child merely being a social embarrassment. Tellingly, these are generic labels for “unsolvable” emotion or mood changes that curiously, require medication to mask, diminish or subdue the “symptoms” of an invented disorder or mental illness. Nice trick!

Echolalia provides a clear example of the perversion of “neutral or normal” process into a “prime” symptom of pathology in the messy, incoherent collage that is promoted as Autism – the big scary threat to American families.

Echolalia

Written by Heaven Stubblefield and Ana GotterMedically Reviewed byKatie Mena, MD on October 28, 2016

From http://www.healthline.com – a popular type of website purporting to provide the “consumer” with information about health topics.

Understanding echolalia:

People with echolalia repeat noises and phrases that they hear.(Here comes the unsupported conclusion that “shifts the defect” into the psycho-social realm) – They may not be able to communicate effectively because they struggle to express their own thoughts. (Or if they are Americans, they may simply not have any original thoughts.)For example, someone with echolalia might only be able to repeat a question rather than answer it. In many cases, echolalia is a (failed or inadequate) attempt to communicate, learn language, or practice language.(Again, the set up of “echolalia” as a deep psycho-social flaw, that “proves” a brain problem exists.)

This is an outrageous escalation of “echolalia” – a behavior that is common in most children, as “enough to prove” a disorder exists.

Repetitive speech is an extremely common part of language development, and is commonly seen in young toddlers who are learning to communicate. By the age of 2, most children will start mixing in their own utterances along with repetitions of what they hear. By age 3, most children’s echolalia will be minimal at most. (Prove that! Echolalia is RAMPANT in American pop-culture as the default communication style and dominates social interaction: repeated catch phrases, memes, and quotes copied over, and over, ad nauseum, especially in attacking and degrading the “status” of other humans! Emojis? )

It’s common for children with autism or developmental delays to have echolaliafurther into childhood (echolia is now posited as a “thing” that one “has” instead of being a specific, changeable or temporary behavior), especially if they’re experiencing delayed speech development. Identifying why and how your child is using echolalia(has it been established that echolalia is intentional?) will help you develop a treatment plan for it.(The authors are already asserting after three paragraphs into the article that your child needs intervention for “a problem”)Consulting a language pathologist can help. $$$$

Symptoms

(Have we established that echolalia – a natural part of speech development, is a disease or a disorder? No. Within the U.S. “helping, caring, fixing” religious movement, any behavior, physical condition or implied mental state qualifies as a potential abnormality.)

The main symptom of echolalia is the repetition of phrases and noises that have been heard. (Echolalia is now a ‘disorder” all by itself!) It can be immediate, with the speaker repeating something right away after hearing it. It can also be delayed, with the speaker repeating something hours or days after hearing it.

This means that any utterance, at any time, can be a symptom of pathology.

Causes and risk factors:Not surprisingly, no causes or risk factors are presented in the Blah, blah, blah below.

Interactive echolalia / Functional echolalia is attempted communication intended to be interactional, acting as communication with another person. (OMG! – Who wrote this?)

Examples include: Turn taking: The person with echolaliauses phrases to fill an alternating verbal exchange. Verbal completion: Speech is used to complete familiar verbal routines that are initiated by others. For example, if people with echolalia are asked to complete a task, they might say “good job!” while completing it, echoing what they’re used to hearing.Providing information:Speech may be used to offer new information, but it may be hard to connect the dots. A mother might ask her child what he wants for lunch, for example, and he’ll sing the song from a lunch meat commercial to say he wants a sandwich.

Non-interactive echolalia / Non-interactive echolalia is typically not intended as communication and is meant for personal use, like personal labeling or self-stimulation. (???) Examples include: Non-focused speech:The person with echolalia says something that has no relevance to the situational (aka “social”)context, like reciting portions of a TV show while walking around a classroom. This behavior may be self-stimulatory. Situation association:Speech is triggered by a situation, visual, person, or activity, and doesn’t seem to be an attempt at communication. If someone sees a brand-name product in the store, for example, they might sing the song from the commercials. Rehearsal:The speaker may utter the same phrase softly to themselves a few times before responding in a normal voice. This may be practice for the coming interaction. Self-direction: People might use these utterances to walk themselves through a process. If they’re making a sandwich, for example, they might tell themselves to “Turn on water. Use soap. Rinse hands. Turn off water. Dry hands. Get bread. Put bread on plate. Get lunch meat,” and so on until the process is completed.

The running commentary of a person’s personal inner voice has been labeled “echolalia” – a far reach from repeating words or phrases as a normal part of language acquisition! Again, any utterance, public or private, may be labeled echolalia, and be construed as “having a disorder”

Interactive vs. non-interactive echolalia: / Echolalia is reflective of how the speaker processes information. (An assumption; not proven) Sometimes, recognizing the difference between interactive and non-interactive echolalia is difficult until you get to the know the speaker and how they communicate. In some cases, echolalia seems completely out of context. (Note again – the move to a non-specific identification of echolalia, “the disorder” as having no objective status: it can be tailored to fit any individual and his or her “suspicious” behavior! By this point, half the readers will likely be assessing themselves, their children, and anyone they know, for having echolalia, the disorder.)

Consider this great example from Susan Stokes. If a child with echolalia gets angry at his teacher when recess is over, he might suddenly say “Go to hell, Lieutenant!” The teacher might later discover that the child had been watching “A Few Good Men” and had used a phrase he knewwas tied to anger(now echolalia is connected to a forbidden emotion)to convey his feelings in that moment. While his response seemed out of context, he had a reason to use that phrase to communicate. (Is this pathological?)

Diagnosing echolalia:

(Echolalia is here assumed to be a proven pathological condition)

A professional can diagnose echolalia by having a conversation with the person with echolalia. If they struggle to do anything other than repeat what has been said, they may have echolalia. Some children with autism are regularly tested for this during their speech lessons. Echolalia ranges from minor to severe. (More properly, a behavior that is a normal part of language acquisition, which may or may not continue in individual people, beyond the “socially acceptable” age. Echolalia may become a minor, or significant, indication of delayed language progression, or MEAN NOTHING AT ALL.) A doctor can identify the stage of echolalia (disease language) and prescribe the appropriate treatment.

Treatment:

Speech therapies: / Some people with echolalia go to regular speech therapy sessions to learn how to say what they’re thinking, (which is actually a forbidden antisocial behavior. What is “wanted” socially is a regurgitation of “proper and normal” social thought.) A behavioral intervention called “cues-pause-point” is often used for intermediate echolalia. In this treatment, the speech therapist asks the person with echolalia to answer a question correctly and tells them they’ll point to them when it’s time to answer. (Gee! Control freak behavior?) Then, the therapist asks a question, such as “What’s your name?” After a short pause, they prompt the speaker to answer. They also hold up a cue card with the correct answer. (Dog-training again!)

Medication: / (Drugs; the modern American psych-psych answer for everything)

A doctor can prescribe antidepressants or anxiety medications to combat the side effects of echolalia. (And just what are these? One of course is being mislabeled as defective.) This doesn’t treat the condition itself, but it helps keep the person with echolalia calm. Since echolalia symptoms may increase when a person is stressed or anxious, the calming effect can help lessen the severity of the condition.

Aye, yai, yai! A rationalization-justification for over-prescribing and off-label use of anti-depressants, not for clinical depression, but “just in case” the person gets upset for any reason. Totally irresponsible and unethical.

Home care: / People with echolalia may work with other people at home to develop their communication skills. There are text and online training programs available to help parents get positive responses from their children.(It’s always about controlling annoying or psycho-socially proscribed behavior. Now we have a normal behavior, echolalia, illegitimately inflated into a global communication – brain deficit that must be corrected by the intervention of “experts” and the pressure to conform placed on the child by their family!) Encouraging a child to use limited vocabulary may make it easier for them to learn to communicate more effectively.

Echolalia outlook and prevention: as if it’s a contagious disease Echolalia is a natural part of language development. It’s not always a good idea to prevent it completely. To avoid permanent echolalia in children, parents must encourage other forms of communication. Expose a child to a wide variety of words and phrases. In time, most children can overcome their echolalia naturally.

Yes, let’s ignore the failure of American education: American public schools are so dysfunctional, that teaching children language mechanics, vocabulary, sentence structure, grammar, etc,, beyond what is necessary for participation in social media, is considered politically incorrect, a waste of time, and constitutes cruel and unusual punishment. The result is that millions of Americans are functionally illiterate, and can’t communicate “what they are thinking” because they aren’t thinking anything, and don’t know how to think.

Cultural echolalia is the expression of neotenic conformity of communication in the U.S., as exemplified in political, media-advertising-marketing, and social media language and images.

According to former US intelligence officials and diplomats, the CIA’s relationship with Saddam Hussein dates back to 1959, when he was part of a CIA-authorized six-man squad that attempted to assassinate Iraqi Prime Minister Abd al-Karim Qasim. (United Press International)

Roger Morris writes of the “regime change” carried out by the CIA in Iraq forty years ago. Among the CIA’s actions were attempted political assassinations and the handing over of a list of suspected communists and leftists that led to the deaths of thousands of Iraqis at the hands of Saddam Hussein’s Ba’ath Party. (New York Times)

In this excerpt from his classic study of Iraqi politics, Hanna Batatu discusses how the Ba`ath Party seized power for the first time in a military coup in February 1963. He speaks of lists, provided by US intelligence, that enabled the party to hunt down its enemies, particularly the Communists, in a terrible bloodletting.

This report by the Senate Banking Committee analyzes the US’s exports of warfare-related goods to Iraq and their possible impact on the health consequences of the Gulf War. The report concludes that the US provided Iraq “with ‘dual-use’ licensed materials which assisted in the development of Iraqi chemical, biological and missile-system programs.” (Gulflink)

According to senior military officials, a covert program carried out during the Reagan Administration provided Iraq with critical battle planning assistance at a time when US intelligence agencies knew that Iraqi commanders would employ chemical weapons against Iran. (New York Times)

The US-backed Iraq Tribunal sentenced Saddam Hussein to death for his role in the 1982 massacre of nearly 150 Shiites in Dujail, Iraq. But the same court has dropped all charges against Hussein, post mortem, for the killing of 180,000 Kurds during the 1980s – crimes committed with Western complicity. The author of this TomPaine piece concludes that if the tribunal does not look into US and British involvement in the genocide case, it will fail “to educate the world about Saddam and his barbarous regime.”

The US-backed Iraq Special Tribunal sentenced the country’s former ruler and “one-time [US] ally” Saddam Hussein to death by hanging – a verdict which came as no surprise to many. The court sought to bring Saddam to justice for crimes against humanity, but failed to acknowledge past US and British administrations’ roles in facilitating these crimes. For decades, Washington provided economic and military support – including chemical weapons – to Saddam’s regime. Therefore, in light of the court’s ruling and its positive reception in Washington, the author of this Independent opinion piece asks, “Have ever justice and hypocrisy been so obscenely joined?”

US Secretary of Defense Donald Rumsfeld has compared critics of the Bush administration’s policy in Iraq to those who appeased Adolf Hitler. The author of this Boston Globe article points out the hypocrisy of such a statement, noting the arming and financing of Saddam Hussein by the Reagan and first Bush administrations. As the article shows, many of the planners of the 2003 Iraq war supported Hussein in the 1980s during his ruthless and genocidal dictatorship.

This Washington Post opinion piece criticizes the historically inconsistent US policy towards Iraq. The author tracks US involvement in Iraq from the 1970s up until the trial of the country’s former leader Saddam Hussein, which began in 2005. Although the US helped to set up the Special Iraq Tribunal, contributing to the exposure of some of these crimes, the author warns against overlooking US complicity with the Hussein regime.

This material highlights the various military, intelligence, and financial assistance given to Saddam’s regime by the US. In 1986, former Vice President George H.W. Bush traveled to the Middle East, repeatedly encouraging Saddam to step up Iraq’s bombing campaign against Iran. In addition, the US supplied Saddam with several big orders of helicopters and provoked a diversionary engagement with the Iranian navy in coordination with a major Iraqi offensive. (Global Policy Forum)

Saddam Hussein’s trial has prompted discussions about US economic and military support to Iraq during the Iran-Iraq War. This bibliography offers a list of sources addressing US policy towards Iraq from 1979 to 1990. (Global Policy Forum)

While the US publicly maintained neutrality during the Iran-Iraq war, it privately attempted to forge a better relationship with the government of Saddam Hussein. This policy did not shift when Iraq used chemical weapons against Iran. (Washington Post)

For decades Washington supported the regime of Saddam Hussein. US officials responsible for such policies could themselves be guilty of war crimes and might face allegations in an international tribunal. (Foreign Policy in Focus)

This report, by the Sustainable Energy and Economy Network, investigates the “revolving door” between the Bechtel Group and the Reagan administration that drove US policy towards Iraq in the 1980s. The authors argue that many of the same actors are back today, justifying military action against Iraq and waiting to reap the benefits of post-war reconstruction.

Britain secretly assisted in building a chemical plant in Iraq despite being fully aware that Saddam Hussein gassed Iranian troops in the 1980s. The warning about possibilities to make chemical weapons was dismissed by Paul Channon, British trade minister at that time, stating abandoning the project “would do our other trade prospects in Iraq no good.” (Guardian)

As part of his call for regime change in Iraq, George W. Bush has accused Saddam Hussein of using poison gas against his own people. However, in 1988 the US worked to prevent the international community from condemning Iraq’s chemical attack against the Kurdish village of Halabja, instead attempting to place part of the blame on Iran. (International Herald Tribune)

As President Reagan’s Middle East envoy in the early 80s, current US Secretary of Defense and leading Bush administration hawk, Donald Rumsfeld, offered support to Saddam Hussein during the Iraq-Iran conflict with knowledge that the Iraqis were using chemical weapons. (Guardian)

This Washington Post article discusses the US role in the military buildup of Iraq preceeding the Gulf War. The administrations of Ronald Reagan and George H.W. Bush authorized the sale of poisonous chemicals and deadly biological viruses such as anthrax and bubonic plague.

The US has always known about Baghdad’s deployment of chemical weapons and their use against his own people, especially during the Iran-Iraq War. “What did the US government do about it then? Nothing,” reports The Nation, “until â€˜gassing his own people’ became a catchy slogan to demonize Saddam.”

This 1991 article discusses the deep intelligence link between the US and Iraq in the 1980s, detailing the intelligence assistance that the US provided to Saddam Hussein during the Iran-Iraq war. (Philadelphia Inquirer)

Former US Ambassador to Iraq Ms. April Glaspie met with Saddam Hussein on July 25 1990, only 8 days before he invaded Kuwait. According to this excerpt from a transcript of their meeting, the two talked about oil prices, how to improve US-Iraq relations, and how the US has “no opinion on the Arab-Arab conflicts, like your border disagreement with Kuwait.” (New York Times)

And so much more: How does the U.S. dare take a “Holier than Thou” attitude toward the rest of the world’s nations?

OMG! The website is: Online Psychology Degree Guide

Wow! Visit the site for the other 22 most influential psychology “experiments” PLUS many other informative lists offering “5 most” to “50 most” lists in this popular pop-social media format.

The 25 Most Influential Psychological Experiments in History

By Kristen Fescoe Published January 2016

“A Class Divided”

Study Conducted By: Jane Elliott

Study Conducted in 1968 in an Iowa classroom

Experiment Details: Jane Elliott’s famous experiment was inspired by the assassination of Dr. Martin Luther King Jr. and the inspirational life that he led. The third grade teacher developed an exercise to help her Caucasian students understand the effects of racism and prejudice.

Elliott divided her class into two separate groups: blue-eyed students and brown-eyed students. On the first day, she labeled the blue-eyed group as the superior group and from that point forward they had extra privileges, leaving the brown-eyed children to represent the minority group. She discouraged the groups from interacting and singled out individual students to stress the negative characteristics of the children in the minority group.

What this exercise showed was that the children’s behavior changed almost instantaneously. The group of blue-eyed students performed better academically and even began bullying their brown-eyed classmates. The brown-eyed group experienced lower self-confidence and worse academic performance. The next day, she reversed the roles of the two groups and the blue-eyed students became the minority group.

At the end of the experiment, the children were so relieved that they were reported to have embraced one another and agreed that people should not be judged based on outward appearances. This exercise has since been repeated many times with similar outcomes.

OMG! It’s ironic that the very studies on which psychologists base their claims are so obviously “super-flawed” that their claim to “be scientists” is easily disproven:

Psychologists claim that use of human subjects as “lab rats” is an ethical “No-No”, but here we see uninformed, not-consenting “captive” children being manipulated (I would call it abuse…) by a teacher! The children suffered distress over the tactics used, including becoming bullies and objects to be bullied. How is this conceptually any different than “punishment” as pedagogy?

The students were “relieved” to be “freed from” this awful manipulation – which automatically is interpreted as instant “moral enlightenment”over the question of physical appearances. This reveals the “social engineering” goals of psychology and the reckless “social puppeteer” attitude that prevails.

This “experiment”(abuse of a word that has specific meaning in science) is “predatory” abuse of power: it may have been “repeated” in various forms (like a “fun prank”) but repetition means that many more children were subjected to manipulation and for no legitimate “reason”.

Car Crash Experiment

Study Conducted by: Elizabeth Loftus and John Palmer

Study Conducted in 1974 at The University of California in Irvine

Experiment Details: Loftus and Palmer set out to prove just how deceiving memories can be. The 1974 Car Crash Experiment was designed to evaluate whether wording questions a certain way could influence a participant’s recallby twisting their memories of a specific event.

And yet, “psychological diagnosis” ARE BASED ON JUST THIS: “self-reporting” or “subjective” opinion of parents, teachers, school counselors, gym teachers, coaches, bystanders and the family dog! A“Psych Wizard”spends three minutes asking “loaded, leading” questions or worse – the “client” is required to fill out a “questionnaire” that is so biased that answers will “reveal” pathology – there are dozens to choose from.

The “researchers” set out to prove what they already know ABOUT THEMSELVES: that manipulation can distort “memories” – it’s their prime directive.

The participants watched slides of a car accident and were asked to describe what had happened as if they were eyewitnesses to the scene. The participants were put into two groups and each group was questioned using different wording such as “how fast was the car driving at the time of impact?” versus “how fast was the car going when it smashed into the other car?” The experimenters found that the use of different verbs affected the participants’ memories of the accident, showing that memory can be easily distorted.

This research suggests that memory can be easily manipulated by questioning technique, meaning that information gathered after the event can merge with original memory causing incorrect recall or reconstructive memory. The addition of false details to a memory of an event is now referred to as confabulation. This concept has very important implications for the questions used in police interviews of eyewitnesses (-and in psychology)

As for the validity of “psychology” having a scientific “fact-finding” interest in assessing human behavior, we can see that the “goal” is to “test” manipulation techniques on human lab rats. It’s utterly non-objective, non-scientific and unethical. Psychologists refuse to be accountable for “proof or results” in theory or practice.

Cognitive Dissonance Experiment

Study Conducted by: Leon Festinger and James Carlsmith

Study Conducted in 1957 at Stanford University

Experiment Details: The concept of cognitive dissonance refers to a situation involving conflicting attitudes, beliefs or behaviors. This conflict produces an inherent feeling of discomfort leading to a change in one of the attitudes, beliefs or behaviors to minimize or eliminate the discomfort and restore balance.

Again, the “basis” is putting humans in situations which manipulate personal morality, group ethics, social obedience, and “pain” in order to find out how these may be “applied” in contexts such as the classroom, workplace, consumer markets, media and advertising – and in government. The conclusion is simple: Lie, and use “bribes” and punishment – the Social Pyramid as we experience it every day. Psychology “intends” to legitimize lies, deception and manipulation as “scientifically valid” in human relationships. This is sick.

Cognitive dissonance was first investigated by Leon Festinger, after an observational study of a cult that believed that the earth was going to be destroyed by a flood. (Christians, perhaps?) Out of this study was born an intriguing experiment conducted by Festinger and Carlsmith where participants were asked to perform a series of dull tasks (such as turning pegs in a peg board for an hour). Participant’s initial attitudes toward this task were highly negative.(Anecdotal, hearsay, subjective opinion, not an “experiment” at all)

They were then paid either $1 or $20 totell a participant waiting in the lobby(lie to them)that the tasks were really interesting.Almost all of the participants agreed to walk into the waiting room and persuade the next participant that the boring experiment would be fun. (The human lab rats were paid to lie and most agreed – where is motivation in this? Were they “students” who always need cash, or individuals who would lie because “an authority figure” asked them to? Who are these human beings ?)

When the participants were later asked to evaluate the experiment, (no, they were asked to evaluate their own experience) the participants who were paid only $1 rated the tedious task as more fun and enjoyable than the participants who were paid $20 to lie.Being paid only $1 is not sufficient incentive for lyingand so those who were paid $1 experienced dissonance. They could only overcome that dissonance by coming to (being lied to) believe that the tasks really were interesting and enjoyable. Being paid $20 provides a reason for turning pegs and there is therefore no dissonance.

OMG! Where do I begin with dissecting this monstrosity of “social logic” and magical thinking?

Like this:

Why did humans evolve big brains? We don’t know, but math can help

Where is the math in this article? You’ll need to go to original paper.

by Kristin Hugo

A new model published Thursday in PLOS Computational Biology mathematically illustrates what led to the evolution of humans’ abnormally large brains. (A cliché that is not true – we have the brain the “fits” us.)

Evolutionary biologists devised these equations to tease apart the relationship between human brain size and the cost of maintaining a large brain. (This is physics: the human body and the evolutionary processes that shaped it, conform to physical laws)Over the last few decades, the pace and stages of brain growth in humans have become clearer. From birth to preschool, our brains quadruple in size. Our brains reach 90 percent of their final size by six years old, and they continue to grow slowly through adolescence until stopping in our mid-20’s.

The question is: Why?

Anthropologists have hypothesized — made educated speculations — about what factors in human evolution drive this pace. For example, newborns heavily rely on their families, so they can develop strong social bonds during their youth. (This is stated as if newborns have the intent to rely on other people, in order to develop social bonds; this is backwards! Human infants must rely on other people because they are helpless. The infant displays behavior that ought to elicit parental bonds, but in fact, there are a very high number of parents who do not respond appropriately – this response ought to be instinctual, but as we commonly see in many domestic animals, this instinctual bond has been interrupted, is undeveloped, or damaged in the mother and other adults)

As humans get older, we increasingly learn to be self-sufficient (or not!); (learn to) use tools and learn about our environments. Scientists speculate both of these habits (?) contribute to brain growth, but they don’t know which of these factors or others have the greatest bearing. We are way off track already – Brain growth depends on NOURISHMENT and adult care – the protection and guidance that will allow the child to learn to “operate” its body, regardless of the society, culture or group size that the infant will grow within.

You’d think that PBS could hire a Competent science writers, or at least employ a science editor! This is piss-poor, garbled reporting! An Asperger pet peeve: If we are going to “educate” the public about scientific Activity, we need Accurate language! Otherwise it’s just Blah, blah, blah.

Anthropologists can plug in their hypotheses to the model (not really) which then predicts brain size from birth to adulthood based on those numbers. If those numbers match what we know about the pace of human brain development, then the model supports the hypothesis. (What numbers? This is gobbled-gook!) “With this model, you can obtain predictions for each of the hypotheses to see which hypothesis yields a better prediction,” said evolutionary biologist Mauricio González-Forero of Université de Lausanne in France, who led the study. Aye, yai, yai!

The final model states that adult skill level equals adult brain mass times the cost of maintaining brain tissue divided by the cost of memory times a constant. Stated in laymen’s terms, this idea means as adult brain mass increases, so too does adult skill, assuming that the costs of maintaining the brain mass and memory stay constant. (Aye, yai, yai!!!!)

These costs include eating a lot in order to maintain the brain. (of the right kind of food)Brains make up 2 percent of our bodies, but consume 20 percent of our oxygen and sugars in our food to sustain the activity of billions of neurons. This mental gorging could have been a disadvantage for early humans thousands of years ago, because bigger diets, consisting of more calories, means having to spend more time hunting and foraging for food. If their evolving brains drained too much food and oxygen, then they might have been too tired to fend for themselves. (Yikes!)

God help us! Another naïve neurotypical narrative!First – this is backwards:IF food X provides more calories per “effort to obtain it” (work), you’re in luck – you will focus on obtaining food X:(bears, sharks, and millions of species do this) For early humans, exploiting a new “option” (such as animal protein) results in more calories, a benefit that then can be maximized by improving and tailoring technology toward getting this food AND for other activities as well. Once this “boost in calories” becomes more available, better brain nourishment (especially in children) provides more “brain power” for developing new technologies and devising better strategies for survival. It’s a feedback process. )

Modern social humans (Americans) seek out “crappy food” that deprives them of the nutrition necessary for even minimal brain and body health. This is bad enough, but to starve our children’s brains is a crime!

While there is debate among anthropologists, many believe that social interaction is a major factor in increasing brain size. Knowing people, communicating with them and maintaining relationships takes a lot of brainpower. This is recent “social narrative” about agricultural societies; regardless of “social” influence, the brain runs on REAL ENERGY supplied by FOOD. What we see in contemporary hyper-social juvenalized humans is overconsumption of “crappy food” which fails to provide adequate nourishment. Compounded by “social demands” that consume too much of a child’s energy, leaves less energy for children to develop healthy brains and bodies: in many children, learning becomes impossible. What we see is a “shrinking” of brain size overthe last 10,000 years of human domestication)

González-Forero’s model counters this narrative and asserts that humans gain more intelligence as they learn to use technology, which University of Wisconsin-Madison evolutionary anthropologist John Hawks describes as a controversial but revealing take on brain development.(Controversial= whacky = magical thinking) Many anthropologists look at the pace of brain growth in terms of social interactions, he added, but “this paper is saying maybe social relationships don’t have anything to do with it.It’s really neat to see such a cool, clear statement of that because it gives us a target.”

The socially-obsessed “naïve narrative” of the evolution of human brain has taken over anthropology and related “human sciences” – at the expense of logical reasoning grounded in the reality of physical environments.

Logically, we can go much further: social activity can be detrimental to human survival, Energy expended on social activity consumes far more energy than it “supposedly” supplies; social activity redistributes food, water and fossil fuels to ultra-greedy nations, thus depriving millions of human beings the “nourishment” that children must have in order to develop. “Saving” children, by handing out “just enough gruel” to keep them alive temporarily, results in underdeveloped and damaged brains, and is unconscionable social activity.

Contemporary humans suffer from this very real food-energy drain. We cannot provide clean water and proper nourishment to hundreds of millions of human children, but “spend” enormous amounts of energy on projects with “no energy return” – war, environmental destruction, and billions of useless products (can’t eat them!), the production of which consumes vast amounts of energy (especially human energy) that is needed for “brain growth”.

Like this:

Epilepsy and Sensory Overload – Adults

Topic:

I have temporal lobe epilepsy with simple partial seizures. I also struggle with something I call sensory overload. I know that is a term for autism, but it is the best way to describe what is happening to me. I have difficulty when there is too much stimulation in the room. I become very agitated if, for example, there is music playing while the TV is on and people are talking. Add too many people to the stimulation and I become very stressed. If I cannot turn off the music and TV, I must leave the room. This agitation and stress is especially strong when I am around children because they tend to create a lot of stimulation with loud voices, banging and thumping from their physical activity, and they lack an understanding for personal space and often run/bump into me. I know too much noise can annoy anyone, but from what I have observed my agitation is much stronger than others in the same situation.

Is the sensory overload problem just another one of my issues or could there be some correlation between that and my epilepsy?

Comment 1.

I don’t know if there is a correlation but people can have Sensory Integration issues. This is not autism although I have read before it could be part of the spectrum. A person can be treated for sensory issues through an occupational therapist with specific training in this area. I am only familiar with therapists who work with children but there must be some out there who would work with adults who were never treated for this as a child. It is worth looking into. There also are books out there that specifically discuss sensory integration issues.

Comment 2.

I think i get something similar. I’m in the process of getting diagnosed with TLE (temporal lobe epilepsy), simple and complex partials. If there is too much to look at, I freak out. Like in shopping centers, all the colors, vastness, noises etc cause me problems. I just wrote in my blog about freaking out while shopping yesterday! I just feel as though I can’t process it all, and its just all too much.

If I am in a simple partial (epileptic seizure) I have to be in complete silence. Even if the TV is on it drives me nuts and I can’t look at anything.

I’m in the beginning stages of diagnosis, but I shall bring this up with my Neuro on my next appointment.

Comment 3.

I am being examined for Temporal Lobe Epilepsy and have also wondered about the Epilepsy and Sensory stuff connection.

I know EXACTLY what you are talking about!!! I call it “Tactile Defensiveness”.

When you said, “….my agitation is much stronger than others in the same situation,” bells went off in my head like “DING DING DING!! THIS IS TOTALLY ME!!”I knew instantly what you are talking about. If my 2 year old rams into my leg (which is like you say entirely normal for his age) I can actually get almost combative. There’s nothing rational about it, I cannot “think” my way out of this reaction. For me it seems to be hard-wired and almost reflexive, the way it would be if a doctor taps your knee with a rubber hammer.

Other “sensory overload” struggles I have:

*the waistband of my clothes often feels too tight, sometimes the socks around my ankles will feel too tight/clingy, sometimes the cuffs/wristband of my jackets will also feel too tight. I simply have to get rid of the offending article of clothes

*I have photosensitivity to many bright lights including sunshine. To compensate, I purchased a nice pair of shades, which happens to be in vogue

*certain cloth has always been aversive to me, in particular polyesther weaves, it was so coarse it felt almost like it scratched my skin. to this day I cannot use bed linen that is not 100% cotton and has a 400 thread count or higher b/c it feels too scratchy on my skin

*places with a lot of lights, sounds, crowds of people, I get panic stricken and overwhelmed, like you said SENSORY OVERLOAD

* cannot wear terry cloth socks b/c it feels to prickly and couldn’t stand the feeling of some face cloths taking a bath as a child

*I am overly sensitive to very hot or very cold temperatures, particularly bath water/shower water

*my shoelaces have to be laced up with the “exact same” tightness on both shoes or I go insane, literally I cannot stand it and have to fix it! LOL

*if I am in a bright store like WalMart sometimes the lights make me well…very on edge almost hair-trigger irritable

*my ears actually hurt when a fire truck puts it’s siren on to the point that when I was a child I would cover them up. As an adult I don’t want to look weird doing that, so I learned to just white knuckle through it with my fist and jaws clenched

*Smells are so strong in my nose that sometimes the scent is so aversive (like dog poo or skunk) that I gag and have to leave a situation. On the other hand pleasant smells are so strong it makes me feel like I’m in heaven if I like it (baking cookies etc) I speculate that I smell more keenly than everyone else

*Taste is the same way but thank God I never had texture issues with food like my sister does.

*If I get something sticky on my hands I have to wash it immediately, I just hate that feeling: maple syrup, jelly/jam

I could go on and on but the bottom line for me, being 36 years old, is that I had to learn to compensate for my heightened sensory issues by either avoiding siutations or de-sensitizing myself. This wasn’t a “formal” process it just happenened out of necessity and I consciously told myself to “sit with the discomfort” I just instinctively knew I had to do it.

Comment 4.

I have been told I self monitor a lot. I used to think this was stupid and ‘as if’, but I can now catch myself in the act. I suppose having a condition like us makes you super sensitive to every bodily sensation that we don’t assume to be normal. In fact, it seems I have decided every bodily sensation is abnormal!

I know there are certain things that my poor little brain doesn’t cope to well with like the whole lights thing, shopping centres, loud noises, heat, being super tired etc … although I think half the time I am so strung out about everything – anything will set me off or freak me out.

I find if its over-cast it sends me in to a tail spin. haha. Weird, hey? I love rainy days, but they make me feel awful. I think I need and respond well to normal natural light / sun shine. i seem to get worse when things get darker. Weird. Hmmm.

OMG! Could the “autism” “brain” “behavior” industry be any more chaotic, incoherent, or ridiculous?

Honestly! Do any of the “experts” ever talk to each other; compare notes, cases, or FACTS? Can they even recognize the vast duplication of diagnosis going on in “parallel universes” of research?

Like this:

Puppies and kittens are cute. Young lions, tigers and bears are cute; adult carnivores are not. Neither are dinosaurs. A manufactured universe of “cute” has invaded children’s entertainment, educational programming, religious indoctrination, clothing, food – and of course, toys. Decades of girls, women (and some boys) think that the Barbie doll was present at the Big Bang.

Cute is a euphemism for infantile and trivial: For too many immature parents, babies are not living beings; they are toys; they are objects to be manipulated to get attention.